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Topics {✒️}

quencher dye 6-carboxy-tetramethyl-rhodamin results identify n-tsp2-fc günter emons & thomas hawighorst n-tsp2-fc-coated wells n-tsp2-fc significantly reduced n-tsp2-fc rapidly decreased n-tsp2-fc-treated mice n-tsp2-fc inhibits reporter dye 6-carboxy-fluorescein n-tsp2-fc-treated tumors n-tsp2-fc inhibited transforming growth factor-beta human mda-mb-435 cells mda-mb-435 cell line mda-mb-435 breast cancer vegf-induced tube formation transforming growth factor-β mda-mb-231 breast carcinomas computer-assisted image analysis mda-mb-435 tumor cells n-tsp2-fc results n-tsp2-fc contained n-tsp2-fc failed recombinant n-tsp2-fc mda-mb-435 tumors grown real-time pcr assay basal-type breast cancers mda-mb-435 tumor growth sided unpaired t-test student–newman–keuls’ test n-terminal recombinant fragment n-tsp2-fc resulted quantitative real-time pcr n-terminal globular domain ncr nu/nu mice n-terminal globular region cd31-stained blood vessels becton-dickinson immunocytometry systems georg-august-university göttingen multi-detection microplate reader mda-mb-435 tumors reached anti-angiogenic thrombospondin-2 variant urokinase-type plasminogen activator human 293-ebna cells article download pdf tumor-bearing mice treated untreated tumor-bearing mice ��ct = ct alu  − ct18srrna recombinant heparin-binding domain xenotransplanted mda-mb-435

Questions {❓}

• Chambers AF (2009) MDA-MB-435 and M14 cell lines: identical but not M14 melanoma?
• Hollestelle A, Schutte M (2009) Comment Re: MDA-MB-435 and M14 cell lines: identical but not M14 Melanoma?

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         headline:CD36-mediated activation of endothelial cell apoptosis by an N-terminal recombinant fragment of thrombospondin-2 inhibits breast cancer growth and metastasis in vivo
         description:Thus far the clinical benefits seen in breast cancer patients treated with drugs targeting the vascular endothelial growth factor (VEGF) pathway are only modest. Consequently, additional antiangiogenic approaches for treatment of breast cancer need to be investigated. Thrombospondin-2 (TSP-2) has been shown to inhibit tumor growth and angiogenesis with a greater potency than the related molecule TSP-1. The systemic effects of TSP-2 on tumor metastasis and the underlying molecular mechanisms of the antiangiogenic activity of TSP-2 have remained poorly understood. We generated a recombinant fusion protein consisting of the N-terminal region of TSP-2 and the IgG-Fc1 fragment (N-TSP2-Fc) and could demonstrate that the antiangiogenic activity of N-TSP2-Fc is dependent on the CD36 receptor. We found that N-TSP2-Fc inhibited VEGF-induced tube formation of human dermal microvascular endothelial cells (HDMEC) on matrigel in vitro and that concurrent incubation of anti-CD36 antibody with N-TSP2-Fc resulted in tube formation that was comparable to untreated control. N-TSP2-Fc potently induced apoptosis of HDMEC in vitro in a CD36-dependent manner. Moreover, we could demonstrate a CD36 receptor-mediated loss of mitochondrial membrane potential and activation of caspase-3 in HDMEC in vitro. Daily intraperitoneal injections of N-TSP2-Fc resulted in a significant inhibition of the growth of human MDA-MB-435 and MDA-MB-231 tumor cells grown in the mammary gland of immunodeficient nude mice and in reduced tumor vascularization. Finally, increased serum concentrations of N-TSP2-Fc significantly inhibited regional metastasis to lymph nodes and distant metastasis to lung as shown by quantitative real-time alu PCR. These results identify N-TSP2-Fc as a potent systemic inhibitor of tumor metastasis and provide strong evidence for an important role of the CD36 receptor in mediating the antiangiogenic activity of TSP-2.
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      headline:CD36-mediated activation of endothelial cell apoptosis by an N-terminal recombinant fragment of thrombospondin-2 inhibits breast cancer growth and metastasis in vivo
      description:Thus far the clinical benefits seen in breast cancer patients treated with drugs targeting the vascular endothelial growth factor (VEGF) pathway are only modest. Consequently, additional antiangiogenic approaches for treatment of breast cancer need to be investigated. Thrombospondin-2 (TSP-2) has been shown to inhibit tumor growth and angiogenesis with a greater potency than the related molecule TSP-1. The systemic effects of TSP-2 on tumor metastasis and the underlying molecular mechanisms of the antiangiogenic activity of TSP-2 have remained poorly understood. We generated a recombinant fusion protein consisting of the N-terminal region of TSP-2 and the IgG-Fc1 fragment (N-TSP2-Fc) and could demonstrate that the antiangiogenic activity of N-TSP2-Fc is dependent on the CD36 receptor. We found that N-TSP2-Fc inhibited VEGF-induced tube formation of human dermal microvascular endothelial cells (HDMEC) on matrigel in vitro and that concurrent incubation of anti-CD36 antibody with N-TSP2-Fc resulted in tube formation that was comparable to untreated control. N-TSP2-Fc potently induced apoptosis of HDMEC in vitro in a CD36-dependent manner. Moreover, we could demonstrate a CD36 receptor-mediated loss of mitochondrial membrane potential and activation of caspase-3 in HDMEC in vitro. Daily intraperitoneal injections of N-TSP2-Fc resulted in a significant inhibition of the growth of human MDA-MB-435 and MDA-MB-231 tumor cells grown in the mammary gland of immunodeficient nude mice and in reduced tumor vascularization. Finally, increased serum concentrations of N-TSP2-Fc significantly inhibited regional metastasis to lymph nodes and distant metastasis to lung as shown by quantitative real-time alu PCR. These results identify N-TSP2-Fc as a potent systemic inhibitor of tumor metastasis and provide strong evidence for an important role of the CD36 receptor in mediating the antiangiogenic activity of TSP-2.
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         Thrombospondin-2
         CD36
         Metastasis
         Angiogenesis
         Oncology
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      name:Institute for Oral and Musculoskeletal Biology, Department of Dermatology, Center for Biochemistry, Center for Molecular Medicine Cologne, Medical Faculty, University of Cologne, Cologne, Germany
      name:Department of Gynecology and Obstetrics, University Medical Center Göttingen, Georg-August-University Göttingen, Göttingen, Germany
      name:Department of Gynecology and Obstetrics, University Medical Center Göttingen, Georg-August-University Göttingen, Göttingen, Germany
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      name:Department of Gynecology and Obstetrics, University Medical Center Göttingen, Georg-August-University Göttingen, Göttingen, Germany

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